Q-omics provides the consensus-scored EFNA5 profile across patient tissues and cancer cell-line models. EFNA5 expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in LUAD. Among the 18 cancer types available for tumor–normal comparison, EFNA5 is differentially expressed in 11, with the highest sampling consensus in LUAD. Additionally, EFNA5 RNA expression shows 17,469 significant gene co-expression associations, with the highest sampling consensus in TGCT. Together, these results highlight LUAD, and TGCT as cancer lineages where EFNA5 shows reproducible signals across survival, tumor–normal expression, and patient cross-omics analyses.
Every result is evaluated using two consensus scores. Sampling consensus measures how consistently a finding is reproduced within a cancer lineage across different conditions. Lineage consensus measures how broadly the result is shared across cancer types, distinguishing pan-cancer signals from lineage-specific patterns.
Premium analyses for EFNA5 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes EFNA5 survival associations across molecular data types. EFNA5 RNA expression shows survival associations in the most cancer types (26), followed by mutation status (2) and mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible EFNA5 RNA expression–survival associations across cancer types. High EFNA5 expression shows unfavorable associations in LUAD, OV, KIRC, KIRP and ACC, but favorable associations in MESO. The LUAD Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p < 0.001). Together, the overview and detailed table identify LUAD as the clearest survival context for EFNA5 RNA expression.
This table summarizes EFNA5 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11, while mass-spec protein shows differences in 4. The strongest signals are observed in THCA for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for EFNA5. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. EFNA5 shows lower tumor expression in THCA, COAD and BRCA and higher tumor expression in LUAD, KICH and CHOL. The LUAD box plot shows higher EFNA5 RNA expression in tumor versus normal tissue (log2 FC = +1.535, t-test p < 0.001).
This table shows molecular features associated with EFNA5 in patient tissues and cancer cell lines. In patient samples, EFNA5 shows the broadest associations at the RNA and protein expression levels, with TGCT recurring as the lineage with the largest associated feature set. In cancer cell lines, EFNA5 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OESOPHAGUS, while CRISPR and shRNA rows add functional-dependency signals in LIVER and UPPER_AERODIGESTIVE_TRACT.
